Background

Mediastinitis is a life-threatening condition that carries an extremely high mortality if recognized late or treated improperly.
[1, 2, 3, 4] Although long recognized as a complication of certain infectious diseases, most cases of mediastinitis are associated with cardiac surgery (>300,000 cases per year in the United States).
[4] This complication affects approximately 1-2% of these patients. Although small in proportional terms, the actual number of patients affected by mediastinitis is substantial. This significantly increases mortality and cost. After 10 years of evolution, the optimal therapy for mediastinitis is more clearly understood.

Future directions for research should focus on prevention, including timely antibiotic administration, sterile technique, prophylactic measures such as topical bacitracin, and meticulous hemostasis. Focus should also include more accurate methods of diagnosis during the first 14 days after surgery, when computed tomography (CT) findings are not reliable. However, the keys to successful management remain early recognition and aggressive treatment, including sternal reopening and debridement. Further research should also focus on the optimal timing and method of wound closure and the duration of antibiotic therapy required for optimal treatment.

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Anatomy

The portion of the thorax defined as the mediastinum extends from the posterior aspect of the sternum to the anterior surface of the vertebral bodies and includes the paravertebral sulci when the locations of specific mediastinal masses are defined. It is limited bilaterally by the mediastinal parietal pleura and extends from the diaphragm inferiorly to the level of the thoracic inlet superiorly.

Traditionally, the mediastinum is artificially subdivided into three compartments for better descriptive localization of specific lesions. When the location or origin of specific masses or neoplasms is discussed, the compartments or spaces are most commonly defined as the anterior, middle, and posterior.

The anterior compartment extends from the posterior surface of the sternum to the anterior surface of the pericardium and great vessels. It normally contains the thymus gland, adipose tissue, and lymph nodes. The physiology of the anterior mediastinum includes the lymphatics and thymus gland. The physiology of the middle mediastinum includes the bronchi, the heart and pericardium, the hila of both lungs, the lymph nodes, the phrenic nerves, the great vessels, and the trachea. The physiology of the posterior mediastinum includes the azygos vein, the descending aorta, the esophagus, the lymph nodes, the thoracic duct, and the vagus and sympathetic nerves.

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Pathophysiology

Infection from either bacterial pathogens or more atypical organisms can inflame any of the mediastinal structures, causing physiologic compromise by compression, bleeding, systemic sepsis, or a combination of these.

The origin of infection following open heart operations is not known in most patients. Some believe that the process begins as an isolated area of sternal osteomyelitis that eventually leads to sternal separation. Others hold that sternal instability is the inciting event, and bacteria then migrate into deeper tissues. Inadequate mediastinal drainage in the operating room may also contribute to the development of a deeper chest infection. The patient's own skin flora and the bacteria in the local surgical environment are possible sources of infection. Because some bacterial contamination of surgical wounds is inevitable, host risk factors are likely critical in promoting an active infection.

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Etiology

Causes

Most cases of mediastinitis in the United States occur following cardiovascular surgery. Risk factors for the development of mediastinitis in this setting include the following:

In general, the use of pedicled bilateral internal mammary artery (BITA) grafts carries increased risk for mediastinitis after coronary artery bypass graft (CABG),
[5] and this risk is even higher among patients with diabetes, thus rendering many surgeons reluctant in using BITA grafting in this subgroup of patients; however, the use of skeletonized BITA grafts may reduce this risk, patients with and without diabetes could be considered for skeletonized BITA
[6]

The frequency of various microbiological pathogens isolated in cases of postoperative mediastinitis.

Fibrosing mediastinitis is most commonly associated with Histoplasma capsulatum and Mycobacterium tuberculosis, though mediastinitis is an extremely rare complication of these infections.
[13]

Acute mediastinitis has also been reported as a complication of Epstein-Barr virus infection.
[16]

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Epidemiology

In the United States, mediastinitis most commonly occurs in the postoperative setting following CABG.
[4] The incidence is 1-2% at most large surgical centers; however, certain subsets of patients, such as patients who have undergone a heart transplant, are at much higher risk.

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Prognosis

The development of mediastinitis dramatically increases mortality and lengthens the hospital stay. One study showed that postoperatively, a patient's chance of dying doubled to 12% when mediastinitis developed compared with 6% for those without the condition. Some studies report death rates as high as 47%. Mediastinitis also raises the 2-year mortality from 2% to 8% following CABG. Patients with postoperative mediastinitis stay in the hospital six to seven times longer than those without the condition, and total costs may triple.
[17]